Antonaccio M J, Kelly E, Halley J
Eur J Pharmacol. 1975 Aug;33(1):107-17. doi: 10.1016/0014-2999(75)90144-2.
In anesthetized dogs, methysergide (1 and 3 mg/kg i.v.) caused reductions in systolic and diastolic blood pressure, heart rate, left ventricular pressure and peripheral resistance. Caardiac output was unchanged because of an increase in stroke volume. Methysergide exhibited no alpha-receptor, ganglion, or adrenergic neuron-blocking properties nor did it have marked direct vasocilator action. The BCO, but not the orthostatic, reflex was severely inhibited by the drug, evidence for a central inhibitory action. Atropine, vagotomy or carotid sinus debuffering had little or no effect on the hypotension and bradycardia produced by methysergide, whereas guanethidine pretreatment essentially abolished these effects. Direct intracerebronventricular administration of small doses of methysergide (0.2 mg/kg) caused significant hypotension and bradycardia. It is concluded that methysergide causes centrally mediated hypotension and bradycardia, the mechanism of which is not clearly understood.
在麻醉犬中，麦角新碱（静脉注射1和3毫克/千克）可导致收缩压和舒张压、心率、左心室压力及外周阻力降低。由于每搏输出量增加，心输出量未发生变化。麦角新碱不具有α受体、神经节或肾上腺素能神经元阻滞特性，也没有明显的直接血管舒张作用。该药物严重抑制了压力感受性反射，但未抑制体位性反射，这证明了其具有中枢抑制作用。阿托品、迷走神经切断术或颈动脉窦去缓冲对麦角新碱引起的低血压和心动过缓几乎没有影响，而胍乙啶预处理基本消除了这些影响。直接脑室内注射小剂量麦角新碱（0.2毫克/千克）可导致明显的低血压和心动过缓。得出的结论是，麦角新碱引起中枢介导的低血压和心动过缓，其机制尚不清楚。
